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AC1 > Cardiac Arrhythmias > Flashcards

Cardiac Arrhythmias Flashcards

1
Q

Define arrhythmias

A

Any variation from the normal rate of rhythm of heart beat

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2
Q

What can the classification of cardiac arrhythmias be based on?

A

Rate

Site of origin

Mechanism

ECG appearance

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3
Q

Describe the phases of cardiac pacemaker cell action potentials

A

Phase 0: Ca2+ in

Phase 3: K+ out

Phase 4: Na+ in, Ca2+ in

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4
Q

Describe the phases of cardiac muscle cell action potentials

A
  • Phase 0: Rapid Na+ influx through open fast Na+ channels
  • Phase 1: Transient K+ channels open; K+ efflux returns TMV to 0mV.
  • Phase 2: Influx of Ca2+ through L-type Ca2+ channels is electrically balanced by K+ efflux through delayed rectifier K+ channels.
  • Phase 3: Ca2+ channels close, delayed rectifier K+ channels remain open and return TMV to -90mV
  • Phase 4: Na+, Ca2+ channels closed. OPen K+ rectifier channels keep TMV stable at -90mV.
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5
Q

Describe normal sinus rhythm

A
  • Rate: 60-100bpm
  • Rhythm: regular
  • P waves: present and preceding each QRS complex
  • PR interval: normal (0.12-0.2 secs)
  • QRS: Normal (<0.12 secs)

Rate and rhythm may vary with respiration (increases on inspiration; decreases on expiration)

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6
Q

What are the 2 main mechanisms of cardiac arrhythmias?

Name examples of each

A

Altered impulse formation

  • Increased automaticity
  • Decreased automaticity

Altered impulse conduction

  • Conduction block
  • Re-entry
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7
Q

What are the cardiac causes of bradycardia?

A
  • Age-related degeneration/fibrosis
  • Infection
  • Ischaemia
  • Cardiomyopathy
  • Congenital
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8
Q

Name some systemic causes of bradycardias

A
  • Drugs
  • Hypothermia
  • Hypothyroidism
  • Electrolyte abnormalities
  • Autonomic dysfunction
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9
Q

Describe sinus bradycardia

A
  • Rate: <60bpm
  • Rhythm: regular
  • QRS, P wave, PR interval all normal
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10
Q

Describe sinus pause/arrest

A
  • Rate: can be normal/slow
  • Rhythm: irregular due to pause
  • P wave, PR interval and QRS all normal

Caused by failure of SA node to fire, therefore the next P wave does not occur at the expected time

Escape rhythms from latent pacemakers may occur during pause

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11
Q

Describe first degree heart block

A

Delayed AV conduction = prolonged PR interval

Often asymptomatic

  • Rate: usually <60bpm
  • Rhythm: regular
  • Usually asymptomatic, no treatment required
  • Normal P wave and QRS complex
  • PR interval prolonged due to delayed conduction
  • No missed beats
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12
Q

Describe second degree heart block type 1

A
  • Rate: Usually <60bpm
  • Rhythm: irregular
  • P wave: present but more P waves than QRS
  • PR interval: progressively prolonged until beat drops
  • QRS normal

Intermittent failure of conduction; PR interval ‘resets’ after each dropped beat and cycle restarts- Wenckenbach phenomenon (Mobitz type 1)

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13
Q

Describe second degree heart block type 2

A
  • Rate: usually <60bpm
  • Rhythm: irregular
  • P wave: present but more P waves than QRS
  • PR interval: normal or prolonged
  • QRS: may be normal or prolonged

Intermittent failure of conduction; constant PR interval.

Can cause palpitations, dizziness, syncope, chest pain, confusion through haemodynamic compromise.

Admit for monitoring, investigate possible ischaemia

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14
Q

Descrive third degree (complete) heart block

A
  • Rate: atrial rate higher than slow ventricular rate (escape rhythm)
  • Rhythm: regular
  • P wave: more P waves than QRS, no clear relationship
  • PR interval: absent (AV dissociation)
  • QRS: normal or broad depending on site of ventricular escape rhythm

Complete failure of conduction; P waves and QRS completely unrelated

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15
Q

How should third degree heart block be managed?

A
  • Cardiac monitoring
  • Atropine
  • Pacing: transcutaneous/temp pacing wire/ PPM
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16
Q

Name some causes of tachycardias

A
  • Anxiety
  • Drugs
  • Alcohol
  • Hyperthyroidism
  • Hypoxaemia
  • Ischaemia
  • Hypotension
  • Electrolyte abnormalities
  • Infection
  • Cardiomyopathy
  • Fibrosis
17
Q

What are the 2 main classifications of tachycardias?

A
  • Supraventricular (arising above the ventricles)
  • Ventricular (arising within the ventricles)
18
Q

Name types of supraventricular tachycardias

A
  • Sinus tachycardia
  • Paroxysmal/ re-entrant SVTs
    • Atrioventricular nodal re-entrant tachycardia
    • Atrioventricular re-entrant (reciprocating) tachycardia
  • Atrial flutter
  • Atrial fibrillation
19
Q

Name types of ventricular tachycardias

A
  • Premature ventricular complex
  • Ventricular tachycardia
  • Ventricular fibrillation
20
Q

Describe sinus tachycardia

A
  • Rate: 100-180bpm
  • Rhythm: regular
  • P waves: present and preceding each QRS
  • PR interval: normal
  • QRS: normal

Usually an appropriate response to an underlying condition

21
Q

Describe paroxysmal/ re-entrant SVTs

A
  • Rate: 140-280bpm
  • Rhythm: normal
  • P waves merged with QRS- retrograde conduction
  • PR interval usually not seen
  • QRS normal

Usually due to re-entry circuit within AV node (AVRNT)- activates both atria and ventricles

May be caused by re-entry circuit using AV node and accessory pathway

22
Q

Describe pre-excitation

A
  • Rate: Normal
  • Rhythm: regular
  • P wave: present and precedes each QRS
  • PR interval: may be short
  • QRS: often broad due to delta wave

= Early activation of the ventricles as impulses bypass AV node via accessory pathway.

Short PR interval and slurring into QRS complex (delta wave)

May give rise to AVRT

Symptomatic patients: Wolff-Parkinson-White syndrome

23
Q

Describe atrial flutter

A
  • Ventricular rate depends on rate of AVN
  • Rhythm: typically regular
  • P wave not seen- flutter ‘F’ waves
  • PR interval not measurable
  • QRS normal
  • Re-entry circuit within atria
24
Q

Describe atrial fibrillation

A
  • Rate: depends on rate of AVN
  • P wave absent
  • Irregular rhythm (intermittent conduction through AVN)
  • Absent PR interval
  • QRS usually normal

Uncoordinated atrial activity: fibrillating waves rather than P waves.

Thromboembolism risk

May be paroxysmal, acute, persistent or permanent

25
Q

Describe Torsade de Pointes

A
  • Fast (200-250 bpm)
  • Irregular rhythm
  • P wave not visible
  • Broad QRS
  • Specific form of polymorphic VT, prolonged QT interval
26
Q

Describe premature ventricular complex

A
  • Underlying rate
  • Irregular rhythm
  • P wave absent during PVC
  • PR interval not measurable during PVC
  • Broad QRS, abnormal morphology

Spontaneous early discharge from ectopic pacemaker in ventricle

27
Q

Describe ventricular tachycardia

A
  • Fast rate (100-250 bpm)
  • Regular rhythm
  • No P wave
  • PR interval not measurable
  • Broad QRS
  • May impair cardiac output (pulseless VT)
  • Can be monomorphic (most common) or polymorphic
28
Q

Describe ventricular fibrillation

A
  • Rate often unmeasurable
  • Irregular rhythm
  • Absent P wave
  • PR interval absent
  • QRS: no organised ventricular activity

Rapid uncoordinated irregular ventricular contractions

Incompatible with adequate cardiac output / pulseless

29
Q

What is automaticity?

A

The property of spontaneous depolarisation, usually only in the SAN, AV and conducting tissues of the heart.

30
Q

What is enhanced automaticity?

What are the 2 types?

A

Other myocardial cells exhibiting automaticity potentially leading to spontaneous depolarisation at sites other than the SAN giving rise to ectopic beats and tachycardias.

Enhanced normal automaticity: accelerated generation of an action potential by normal pacemaker tissue.

Abnormal automaticity: accelerated generation of an action potential by abnormal tissue within the myocardium.

31
Q

Which factors may enhance automaticity?

How do these factors cause enhanced automaticity?

A
  • Catecholamine excess
  • Ischaemia
  • Abnormal pH
  • Electrolyte abnormalities

Enhanced automaticity may be caused by factors that decrease the threshold or increase the slope of phase 4 depolarisation.

32
Q

What is triggered activity?

A

Triggered activity results from the premature activation of cardiac tissues by afterdepolarisations, which are depolarizations triggered by one or more preceding action potentials.

These afterdepolarisations can be early (before full repolarisation- phase 2-3) or delayed (after full repolarisation- phase 4 of the cardiac cycle).

The new AP generated can then generate another AP leading to sustained triggered activity.

33
Q

What is re-entry?

How does it differ from normal conduction?

What types of arrhythmias does re-entry underlie?

A

Normal conduction usually results in uniform spread of depolarisation in a constant direction.

Re-entry occurs when the depolarisation wave is able to form a self-propagating looped circuit.

Underlies tachycardias including:

  • Atrial flutter
  • Re-entrant tachycardias (AVNRT and AVRT
  • Some ventricular tachycardias
34
Q

What are the pre-requisites for ‘classic’ re-entry to occur?

A
  • At least two pathways or the presence of a barrier along the conduction pathway
  • Unidirectional block in one of the pathways
  • Conduction must be slow enough (and/or refractory period short enough) to prevent the depolarisation wave encountering refractory tissue within the circuit
35
Q

What is occuring in these images of re-entry?

A

In (1) the impulse passes down both limbs of the potential tachycardia circuit (normal conduction).

In (2) the impulse is blocked in one pathway (α) (e.g. still in refractory phase), but proceeds slowly down pathway β, returning along pathway α until it collides with refractory tissue.

In (3) the impulse travels so slowly along pathway β that it can return along pathway α and complete the re-entry circuit, producing a circus movement tachycardia.

36
Q
A

AC1 (32 decks)

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